ARRHYTHMIAS TACHYCARDIA>100/min BRADYCARDIA<50/min CARDIAC ARREST Electrical activity –ChaoticVF –Absentasystole

Action potential -60 0

Propagating action potential -60 0

Propagating action potential -60 0

Propagating action potential -60 0

Propagating action potential -60 0

Propagating action potential

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

DEPOL Inward  REPOL outward 

Propagating action potential

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

DEPOL Inward  REPOL outward 

DEPOL Inward  REPOL outward 

AUTOMATICITY Physiological: Sinus node Pathological: Reduction/depolarisation of resting membrane potential (e.g. Ischaemia)

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

Tachyarrhythmias Antiarrhythmic drugs –Vaughan-Williams Classification –Drugs divided according to EP effects on cells –All are negatively inotropic –Can also be pro-arrhythmic

Tachyarrhythmias Class I –Impede Na transport across cell membrane –Ia increase AP duration eg quinidine, disopyramide, procainamide –Ib shorten AP duration eg lignocaine, mexilitene, propafenone –Ic little effect on AP eg flecainide

Tachyarrhythmias Class II –Interfere with effects of SNS on the heart eg beta blockers Class III –Prolong AP duration but do not effect initial Na dependent phase eg sotalol, amiodarone Class IV –Antagonise Ca transport across cell membrane –SA and AV node particularly susceptible eg verapamil, diltiazem

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

AV Nodal block [Class II –Interfere with effects of SNS on the heart eg beta blockers] Class III –Prolong AP duration but do not effect initial Na dependent phase eg sotalol, amiodarone Class IV –Antagonise Ca transport across cell membrane –SA and AV node particularly susceptible eg verapamil, diltiazem Adenosine –Specific AV nodal block

EP study: standard fixed wires

RADIOFREQUENCY ABLATION

TREATMENT STRATEGY STABILISE AUTOMATICITY PROLONG ACTION POTENTIAL SLOW CONDUCTION INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

RFA: success rates AVJ98% AVNRT97% AP93% (L 95%, R 89%) AFl95% Infarct VT60-90%, long term 50% Idiopathic VT90% Focal AF60%

RFA: treatment of choice AVJ98% AVNRT97% AP93% (L 95%, R 89%) AFl95% Idiopathic VT90% ______________________________ ?Infarct VT60-90%, long term 50% ?Focal AF60%

Atrial flutter

Atrial Flutter: RFA vs AA drugs JACC2000;35:1898 prospective, randomised – 61 pts SR at 21 months:36%AAD vs 80% RFA Rehospitalised:63% AAD vs 22% RFA AF:53% AAD vs 29% RFA QOL:no change AAD improvement RFA

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

Concepts of AF: MULTIPLE WAVELETS Ines, Garrey MOTHER WAVE Lewis HYPEREXCITABILITY Engelmann, Winterberg

WPW syndrome

AV re-entry tachycardia

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

Ventricular tachycardia

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

Rhythm Strip During Episode of Sudden Death

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

Implanatable defibrillators

Implanatable defibrillator in-situ

Sinus node disease

AV node disease 1st degree heart block 2nd degree heart block (2:1)

AV node disease Complete (3rd degree) heart block

Bradyarrhythmias AV node disease –1st degree; prolonged PR interval –2nd degree; Mobitz type I (Wenckebach); increasing PR interval then non-conducted P wave –2nd degree; Mobitz type II; non-conducted P waves –2nd degree; 2:1 or 3:1 AV node block –3rd degree; complete heart block AV block usually caused by idiopathic fibrosis; other causes include MI, drugs and congenital block

TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

Bradyarrhythmias Treatment of symptomatic bradyarrhythmias often consists of pacing In the short-term drugs may be used to augment conduction eg atropine, isoprenaline